The compliance of arterial tissue to pulse-pressure-volume deformations results from the anatomic arrangements and the intrinsic tensile properties and unrestricted movements of elastin, smooth muscle and collagn elements within the artery wall. The tensile properties of elastin and collagen are dependent in part upon their quantity and their degree of cross-linking. Restrictions in movements (accentuated anisotropism) occur at sites of multidirectional branching or in regions of muscle or bony encumbrances to cause focal increase in glycosaminoglycan and collagen deposition. The underlying hypothesis of this research is that sex differences in age-related and atherogenic lesions in arteries in man reflect an androgen-mediated potentiation of accentuated anistropism and its resonse and that the androgen effect begins in the neonatal and prepubertal periods. The overall objectives of the studies, therefore, are to: (1) identify an androgen imprint on arterial wall elastin (and collagen) occuring during the early developmental period that will influence the biomechanical properties of the tissue in the adult period; and (2) discover pharmacologic means of modifying the androgen imprint. Using Sprague-Dawley rats, we find a temporal coincidence between the largest sex differences in circulating androgens and the maximum differences in the qualitative and quantitative levels of isodesmosine (Ide) and desmosine (Des) cross-links of aortic elastin. The emerging outline of an androgn imprint is: (1) decreased levels of borohydride-reducible Ide and Des; (2) an increased density of non-reducible Ide and Des; and (3) a greater collagen concentration. Elements of the imprint are seen in the neonates and are more completely expressed at 60 days.